A possible role of vitamin D in the genesis of parenteral-nutrition-induced metabolic bone disease.
Patients receiving long term parenteral nutrition may develop metabolic bone disease. In all 11 patients studied, histologic studies of bone showed excessive unmineralized bone tissue despite normal plasma 25-hydroxyvitamin D levels. Three patients also had bone pain and fractures and severe urinary loss of calcium and phosphate. Withdrawal of vitamin D from parenteral nutrition solutions was associated with improved histologic findings of bone in all patients, shown by a decrease in osteoid tissue and an increase in tetracycline uptake. In the three patients with symptoms, bone pain subsided, fractures healed, and urinary loss of calcium and phosphate decreased. Thus, vitamin D may be a factor in the genesis of parenteral nutrition-induced metabolic bone disease.
D015652:25-Hydroxyvitamin D 2; D000328:Adult; D001851:Bone Diseases, Metabolic / Q000209:etiology*; D001842:Bone and Bones / Q000473:pathology; D002118:Calcium / Q000378:metabolism; D004100:Dihydroxycholecalciferols / Q000097:blood; D004872:Ergocalciferols / Q000008:administration & dosage / Q000009:adverse effects* / Q000031:analogs & derivatives / Q000097:blood; D005260:Female; D005459:Fluorides / Q000378:metabolism; D006801:Humans; D008297:Male; D008875:Middle Aged; D010018:Osteomalacia / Q000209:etiology; D010288:Parenteral Nutrition / Q000009:adverse effects*; D010289:Parenteral Nutrition, Total / Q000009:adverse effects*; D010710:Phosphates / Q000378:metabolism
D004100:Dihydroxycholecalciferols; D004872:Ergocalciferols; D010710:Phosphates; D015652:25-Hydroxyvitamin D 2; D005459:Fluorides; D002118:Calcium